Hepatic injuries attributable to terbinafine usage are a well-documented yet infrequent phenomenon. This case study details the clinical presentation and management of a 70-year-old Hispanic female, with no previous medical history, subsequently hospitalized for progressive jaundice, right upper quadrant abdominal discomfort, and worsening pruritus. A comprehensive review of her prior records revealed a recent terbinafine prescription for onychomycosis, which she took consistently for five weeks and then self-discontinued four weeks before her current admission. Laboratory tests on admission revealed a cholestatic pattern of liver injury, evident by transaminitis and conjugated hyperbilirubinemia. The R factor used to determine whether a liver injury is hepatocellular or cholestatic was 0.9. Further diagnostic imaging, including abdominal ultrasound, CT of the abdomen, and magnetic resonance cholangiopancreatography, failed to disclose an obstructive pathology, revealing only cholelithiasis and chronic cholecystitis. Therapeutically, the patient was initiated on hydroxyzine to address symptoms of pruritus, and then subsequently underwent a liver biopsy. Histopathologic findings from the biopsy revealed benign hepatic parenchyma demonstrating focal canalicular cholestasis, mild chronic inflammation involving select portal tracts, and chronic lobular inflammation, suggesting terbinafine-induced hepatotoxicity. This case highlights the challenges of diagnosing terbinafine-induced liver injury, emphasizing the need for a high index of clinical suspicion and recognizing the potential for prolonged symptomatic manifestation after drug discontinuation. This article provides valuable insights into the complexities inherent in such diagnoses and significantly enriches a medical provider's approach to diagnosing and treating unexplained liver injuries.
Keywords: cholestatic liver injury; conjugated hyperbilirubinemia; drug-induced liver injury; liver toxicity; terbinafine.
Copyright © 2023, Jilani et al.